Recognition of erectile dysfunction (ED) as an early sign of systemic cardiovascular disease offers an opportunity for prevention. Cardiac risk assessment may deserve measurement of Apolipoprotein B/Apolipoprotein A-1 ratio. An elevated ApoB/ApoA-1 ratio is a risk factor for future coronary artery disease. ApoA-1 production, which is recognized as a cardioprotective lipid fraction, is down regulated by NFκB activation in vitro. Because inhibition of phosphodiesterases (PDEs) 5, 6 and 9 negatively attenuates NFκB translocation/activation, tadalafil, a selective PDE 5 inhibitor used for treatment of ED could present some interesting pleiotropic effects. The objective of this open study is to test the hypothesis that tadalafil treatment could decrease serum ApoB/ApoA-1 ratio.
Material and methods
Ten healthy men without any complain of ED or known cardiovascular risk factors were administered tadalafil 10mg intake on alternate days for 4 weeks. Lipid profile with total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, ApoA-1 and ApoB, was assessed at baseline (T0), after 2weeks (T1), at the end of the treatment period (T2) and after 2weeks of wash-out follow-up (T3).
ApoB/ApoA-1 ratio was significantly decreased during treatment (mean±SEM, T0: 0.80±0.11, T1: 0.64±0.06, T2: 0.65±0.06; p <0.05) and remained lower after wash-out (T3: 0.67±0.05; p =0.08). Serum ApoA-1 (mg/dl) increased but not significantly during the treatment period (15.2±8.8, 16.5±7.9, 16.9±6, 15.3±7, p =0.26) and ApoB (mg/dl) significantly decreased (11.7±10.8, 10.3±8.4, 10.6±9.9, 10.2±8.6, p =0.03). HDL and LDL cholesterol were unchanged.
This preliminary study showed the interest of PDE 5 inhibitors to decrease the cardiac risk factor ApoB/ApoA-1 ratio. Randomised controlled studies with longer follow-up are needed to confirm those results.